During the current fiscal year (2008) we found:[unreadable] [unreadable] (1) Incubation of naive (CD43-) spleen B cells ex-vivo in the absence of BCR cross-linking ligands resulted in time-dependent expression of p100, the protein product of the NF&#954;B2 gene.[unreadable] [unreadable] (2) p100 up-regulation was blocked by two different pharmacologic inhibitors of the tyrosine kinase, Syk, indicating that it is the result of active signaling downstream of the BCR.[unreadable] [unreadable] (3) B cells treated with Syk inhibitors did not respond to BLys-dependent survival; our interpretation is that long-term survival in response to BLys require ongoing p100 synthesis mediated by tonic BCR signaling. p100 up-regulation was significantly amplified by acute cross-linking of the BCR and blocked by inhibitors of the classical NF-&#954;B pathway.